止血帶休克后主動(dòng)脈收縮反應(yīng)性及RAS成分的變化
發(fā)布時(shí)間:2018-02-25 16:40
本文關(guān)鍵詞: 止血帶休克 主動(dòng)脈 血管收縮反應(yīng)性 腎素-血管緊張素系統(tǒng) 出處:《中國(guó)病理生理雜志》2016年03期 論文類型:期刊論文
【摘要】:目的:通過(guò)觀察止血帶休克(tourniquet shock,TS)后主動(dòng)脈收縮反應(yīng)性及腎素-血管緊張素系統(tǒng)(renin-angiotensin system,RAS)的變化,探討RAS穩(wěn)態(tài)失衡在止血帶休克后主動(dòng)脈低反應(yīng)性及損傷中的作用。方法:8月齡C57BL/6的雄性小鼠,分為對(duì)照組及6個(gè)模型組,每組6只。模型組進(jìn)行止血帶套扎雙后肢阻斷血流,2h后解套扎進(jìn)行再灌注,分別于再灌注10 min、1 h、2 h、4 h、6 h和12 h后處死,對(duì)照組不進(jìn)行套扎與再灌注,其余操作同模型組;多普勒血流儀測(cè)定肢體血流,頸動(dòng)脈插管法測(cè)定平均動(dòng)脈壓(MAP),離體血管張力測(cè)定儀測(cè)定主動(dòng)脈收縮反應(yīng)性,HE染色結(jié)合透射電鏡評(píng)價(jià)血管形態(tài)學(xué)損傷;Western blot檢測(cè)血管組織中血管緊張素Ⅱ1型受體(AT1受體)、血管緊張素(1-7)受體(Mas受體)、血管緊張素轉(zhuǎn)換酶(ACE)和ACE2蛋白的表達(dá)。采用ELISA檢測(cè)血清中血管緊張素Ⅱ(AngⅡ)和血管緊張素(1-7)[Ang(1-7)]的含量。結(jié)果:與對(duì)照組相比,模型組出現(xiàn)下述變化:(1)隨著再灌注時(shí)間的延長(zhǎng)血流量逐漸減少;MAP在再灌注10 min明顯升高,隨后逐漸降低;血管對(duì)去甲腎上腺素的反應(yīng)性在再灌注10 min升高隨后下降,再灌注4 h的血管反應(yīng)性最低;形態(tài)學(xué)損傷評(píng)分隨再灌注時(shí)間延長(zhǎng)逐漸增高;(2)主動(dòng)脈AT1受體與ACE2蛋白表達(dá)逐漸下降,Mas受體與ACE蛋白表達(dá)逐漸升高;(3)血清中AngⅡ的含量整體呈升高趨勢(shì),Ang(1-7)的含量整體呈降低趨勢(shì)。結(jié)論:主動(dòng)脈收縮反應(yīng)性在休克初期暫時(shí)升高,隨后降低,其發(fā)生機(jī)制可能與血管形態(tài)學(xué)損傷及RAS失衡有關(guān)。
[Abstract]:Objective: to observe the changes of aortic contractile reactivity and renin-angiotensin system (RASs) after tourniquet shock in tourniquet TS. To investigate the role of RAS homeostasis in aortic hyporesponsiveness and injury after tourniquet shock. Methods male mice at the age of 8 months C57BL / 6 were divided into two groups: control group and 6 model groups. 6 rats in each group were treated with tourniquet ligation and ligation of hind limbs for 2 h, then released for reperfusion. The rats in the model group were killed at 10 min, 1 h, 2 h, 4 h, 4 h, 6 h and 12 h, respectively. The control group did not perform ligation and reperfusion, while the rest operated the same as the model group. The blood flow of limbs was measured by Doppler flow meter. The mean arterial pressure was measured by carotid artery catheterization, the vasoconstrictive reactivity of aorta was measured by in vitro vasotension apparatus, and the vascular morphological damage was evaluated by HE staining combined with transmission electron microscope. Western blot was used to detect angiotensin 鈪,
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